001     140922
005     20240321220912.0
024 7 _ |a 10.1007/s12035-018-1444-7
|2 doi
024 7 _ |a pmid:30539330
|2 pmid
024 7 _ |a pmc:PMC6647430
|2 pmc
024 7 _ |a 0893-7648
|2 ISSN
024 7 _ |a 1559-1182
|2 ISSN
024 7 _ |a altmetric:52597083
|2 altmetric
037 _ _ |a DZNE-2020-07244
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Weise, Stefan C
|b 0
245 _ _ |a FOXG1 Regulates PRKAR2B Transcriptionally and Posttranscriptionally via miR200 in the Adult Hippocampus.
260 _ _ |a Totowa, NJ
|c 2019
|b Humana Press
264 _ 1 |3 online
|2 Crossref
|b Springer Science and Business Media LLC
|c 2018-12-11
264 _ 1 |3 print
|2 Crossref
|b Springer Science and Business Media LLC
|c 2019-07-01
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1591185830_20666
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a Rett syndrome is a complex neurodevelopmental disorder that is mainly caused by mutations in MECP2. However, mutations in FOXG1 cause a less frequent form of atypical Rett syndrome, called FOXG1 syndrome. FOXG1 is a key transcription factor crucial for forebrain development, where it maintains the balance between progenitor proliferation and neuronal differentiation. Using genome-wide small RNA sequencing and quantitative proteomics, we identified that FOXG1 affects the biogenesis of miR200b/a/429 and interacts with the ATP-dependent RNA helicase, DDX5/p68. Both FOXG1 and DDX5 associate with the microprocessor complex, whereby DDX5 recruits FOXG1 to DROSHA. RNA-Seq analyses of Foxg1cre/+ hippocampi and N2a cells overexpressing miR200 family members identified cAMP-dependent protein kinase type II-beta regulatory subunit (PRKAR2B) as a target of miR200 in neural cells. PRKAR2B inhibits postsynaptic functions by attenuating protein kinase A (PKA) activity; thus, increased PRKAR2B levels may contribute to neuronal dysfunctions in FOXG1 syndrome. Our data suggest that FOXG1 regulates PRKAR2B expression both on transcriptional and posttranscriptional levels.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
|0 G:(DE-HGF)POF3-342
|c POF3-342
|f POF III
|x 0
542 _ _ |i 2018-12-11
|2 Crossref
|u https://creativecommons.org/licenses/by/4.0
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Cyclic AMP-Dependent Protein Kinase RIIbeta Subunit
|2 NLM Chemicals
650 _ 7 |a Forkhead Transcription Factors
|2 NLM Chemicals
650 _ 7 |a Foxg1 protein, mouse
|2 NLM Chemicals
650 _ 7 |a MicroRNAs
|2 NLM Chemicals
650 _ 7 |a Mirn200 microRNA, mouse
|2 NLM Chemicals
650 _ 7 |a Nerve Tissue Proteins
|2 NLM Chemicals
650 _ 7 |a PRKAR2B protein, human
|2 NLM Chemicals
650 _ 2 |a Age Factors
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Cyclic AMP-Dependent Protein Kinase RIIbeta Subunit: genetics
|2 MeSH
650 _ 2 |a Cyclic AMP-Dependent Protein Kinase RIIbeta Subunit: metabolism
|2 MeSH
650 _ 2 |a Forkhead Transcription Factors: genetics
|2 MeSH
650 _ 2 |a Forkhead Transcription Factors: metabolism
|2 MeSH
650 _ 2 |a Hippocampus: growth & development
|2 MeSH
650 _ 2 |a Hippocampus: metabolism
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Mice, Transgenic
|2 MeSH
650 _ 2 |a MicroRNAs: genetics
|2 MeSH
650 _ 2 |a MicroRNAs: metabolism
|2 MeSH
650 _ 2 |a Nerve Tissue Proteins: genetics
|2 MeSH
650 _ 2 |a Nerve Tissue Proteins: metabolism
|2 MeSH
650 _ 2 |a Transcription, Genetic: physiology
|2 MeSH
700 1 _ |a Arumugam, Ganeshkumar
|b 1
700 1 _ |a Villarreal, Alejandro
|b 2
700 1 _ |a Videm, Pavankumar
|b 3
700 1 _ |a Heidrich, Stefanie
|b 4
700 1 _ |a Nebel, Nils
|b 5
700 1 _ |a Dumit, Verónica I
|b 6
700 1 _ |a Sananbenesi, Farahnaz
|0 P:(DE-2719)2811099
|b 7
|u dzne
700 1 _ |a Reimann, Viktoria
|b 8
700 1 _ |a Craske, Madeline
|b 9
700 1 _ |a Schilling, Oliver
|b 10
700 1 _ |a Hess, Wolfgang R
|b 11
700 1 _ |a Fischer, Andre
|0 P:(DE-2719)2000047
|b 12
|u dzne
700 1 _ |a Backofen, Rolf
|b 13
700 1 _ |a Vogel, Tanja
|0 P:(DE-HGF)0
|b 14
|e Corresponding author
773 1 8 |a 10.1007/s12035-018-1444-7
|b : Springer Science and Business Media LLC, 2018-12-11
|n 7
|p 5188-5201
|3 journal-article
|2 Crossref
|t Molecular Neurobiology
|v 56
|y 2018
|x 0893-7648
773 _ _ |a 10.1007/s12035-018-1444-7
|g Vol. 56, no. 7, p. 5188 - 5201
|0 PERI:(DE-600)2079384-4
|n 7
|q 56:7<5188 - 5201
|p 5188-5201
|t Molecular neurobiology
|v 56
|y 2018
|x 0893-7648
856 7 _ |2 Pubmed Central
|u http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6647430
909 C O |o oai:pub.dzne.de:140922
|p VDB
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 7
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 12
|6 P:(DE-2719)2000047
913 1 _ |a DE-HGF
|b Forschungsbereich Gesundheit
|l Erkrankungen des Nervensystems
|1 G:(DE-HGF)POF3-340
|0 G:(DE-HGF)POF3-342
|2 G:(DE-HGF)POF3-300
|v Disease Mechanisms and Model Systems
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914 1 _ |y 2019
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LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21